著者

吉村 博之

出版者

The Japanese Society for Hygiene

雑誌

日本衛生学雑誌 (ISSN:00215082)

巻号頁・発行日

vol.37, no.6, pp.848-865, 1983-02-28 (Released:2009-02-17)

参考文献数

83

被引用文献数

1 1

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The increase in the standard population death rate from pulmonary cancer warrants attention. Three factors can be attributed to this increase: air pollution, cigarette smoking, and occupational exposure to carcinogens. The present paper reports on the results of a study of the relationship between air pollution and pulmonary cancer. Rats, mice, and hamsters were subjected to up to 12 months exposure to diluted gasoline engine exhaust containing 300±50ppm CO, 0.21ppm NO, 0.08ppm NO2, 28ppmC hydrocarbon in the form of methane and 32ppb O3. Further experimentation consisted of combined treatments with carcinogens-rats with diisopropanolnitrosamine, mice with ethylcalbamate, and hamsters with diethylnitrosamine to determine whether the incidence of tumors would increase. No animals exposed exclusively to exhaust gas diveloped pulmonary tumors, indicating that exhaust caused no lung tumorigenesis. However, the frequency of pulmomary tumors increased in animals subjected to combinations of exhaust and carcinogens. The incidence of malignant pulmonary tumors in the rats group exposed for 12 months to carcinogens only was 8.7%, while that in the group exposed to the combination was 30.3%, with the rates for mice 72.7% as against 91.7%, and for hamsters, 3.8% as against 10%. The results indicate that gasoline engine exhaust increases the development of lung tumors, and that exhaust plus other carcinogens significantly increases the risks.

著者

吉村 博之 竹本 和夫

出版者

公益社団法人日本産業衛生学会

雑誌

産業医学 (ISSN:00471879)

巻号頁・発行日

vol.33, no.2, pp.81-93, 1991-03-20

被引用文献数

1

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Occupationally induced lung cancer and mesothelioma have long been attributed to asbestos and moreover, several epidemiological studies have indicated a co-carcinogenic effect of cigarette smoking on the incidence of lung cancer in asbestos workers. The aim of the present study was to investigate the co-carcinogenic effects of asbestos and other carcinogens with emphasis placed on determining the effects of cigarette smoking on the incidence of asbestos induced carcinomas. Doses of 15mg of chrysotile asbestos were administered intratracheally to Wistar rats alone and in conjunction with N-bis(hydroxypropyl)nitrosamine (DHPN) and/or cigarette smoking. DHPN at dose of 1g/kg/B.W. was injected three times intraperitoneally, and the subject animals were exposed to smoke from 10 cigarettes per day, six days a week, for their entire life span. As a result, lung carcinomas were induced in one out of the 31 rats receiving only asbestos. Lung tumors were induced at a much higher incidence in the groups receiving DHPN alone and in conjunction with asbestos: of the 37 rats treated with DHPN alone 19 (51.4%) developed lung tumors, whereas those receiving asbestos as well showed an incidence of 68.4% (23/38) of carcinomas. The development of lung carcinomas (including adenocarcinomas, epidermoid carcinomas, anaplastic carcinomas, and combined carcinomas) was seen in 8 (21.6%) out of the 37 rats receiving DHPN alone and in 23 (60.5%) out of the 38 rats receiving asbestos as well. The incidence of lung carcinoma was significantly increased in combined treatment with asbestos than DHPN alone. In the group receiving asbestos in combination with cigarette smoke, 4 (13.8%) out of the 29 rats developed lung carcinomas, but these carcinomas were more common than in the group receiving only asbestos. Moreover, in the group administered asbestos, DHPN and smoking combined, lung tumors developed in 18 (62.1%) out of the 29, 15 (51.7%) of which proved to be malignant. Mesothelioma (pleura) was induced in three groups in the following combinations: DHPN plus asbestos, 8/38 (21.17%); smoking plus asbestos, 2/29 (6.9%); and smoking, DHPN and asbestos, 4/29 (13.8%). These tumors were extensively located, that is, on the parietal pleura, visceral pleura, epicardium and diaphragm surface. However, mesothelioma was not induced by asbestos alone nor by DHPN alone. Carcinogenicity of asbestos for pleural tumors was significantly promoted by combined treatment with DHPN to an extent greater than DHPN alone. It should be noted that asbestos plus smoking resulted in a higher incidence of mesothelioma than asbestos alone. The results of this study suggest that asbestos can induce lung cancer and that cigarette smoking has a promoting effect on asbestos-induced cancer and mesothelioma as well. Additionally, it was observed that the development of lung tumors and their malignancy and mesothelioma by asbestos is synergistic ally increased by the combined administration of DHPN. There were some histological differences in the carcinomas induced by DHPN alone and those induced in conjunction with asbestos.